Method of treating periodontal disease

ABSTRACT

The present invention includes a method for treating periodontal disease. The method comprises delivering to a pocket of a tooth with periodontal disease, a viscous, reddish-brown solution comprising sulfuric acid and sulphonated phenolic compounds. The method also comprises retaining the reddish-brown solution in the pocket for t time ranging from about 5 seconds to about 60 seconds.

BACKGROUND OF THE INVENTION

The present invention relates to a method for treating periodontaldisease.

Periodontal disease is characterized by a loss of supporting tissues ofthe teeth. In particular, periodontitis includes a loss of theperiodontal ligament and a disruption of the ligament attachments tocementum, as well as reabsorption of alveola and bone. Along with a lossof tissue attachments, periodontal disease produces a migration of theepithelial attachments along the root surface and reabsorption of bone.

It is widely accepted that an initiation and progression of periodontaldisease is dependent upon the presence of micro-organisms which arecapable of causing the disease. At least three characteristics ofperiodontal micro-organisms have been identified which contribute to theability of microbes to act as pathogens. A first characteristic is acapacity of the microbes to colonize. A second characteristic is anability of the microbes to evade anti-bacterial host defense mechanisms.A third characteristic is an ability of the microbes to producesubstances which directly initiate tissue destruction.

Two major periodontal disease pathogens, A. actinomycetemcomitans and P.gingivalis, are able to invade into the tissues. A.actinomycetemcomitans passes through epithelial cells into theunderlying connective tissue while P. gingivalis invades and persists inepithelial cells.

It is believed that direct pathological effects of bacteria and effectsof their products on the periodontium are significant during earlystages of periodontal disease. Analysis of plaque samples from patientswith increasingly severe levels of gingival inflammation reveals asuccession of bacterial species with an increased capacity to directlyinduce an inflammatory response. For example, an increase in persistentlevels of Fusobacterium nucleatum incites a mild gingivitis. Asubsequent production of its metabolic by-products directly effectsgingival vasculature. Resulting edema and an increase in production of,gingival crevicular fluid, GCF, provides an environment and nutrientsthat allow putative pathogens to flourish.

Bacteria such as P. gingivalis also produce enzymes such as proviasis,collagenase, and fibrinolysin that directly degrade surrounding tissuesin superficial layers of the periodontium. In addition, this bacteriumproduces metabolic by-products such as H₂S, ammonia and fatty acids thatare toxic to surrounding cells. Furthermore, bacterial constituents suchas lipopolysaccharide are capable of inducing bone reabsorption invitro.

Once major protective elements of the periodontium have been overwhelmedby bacterial virulence mechanisms, several host-mediated destructiveprocesses are initiated. Polymorphonucleocytes (PMNS), which normallyprovide protection can themselves contribute to tissue pathology. Duringa process of phagocytosis, PMNs typically spill some of the enzymecontent extracellularly during a process known as degranulation. Some ofthe enzymes are capable of degrading the surrounding host tissues, suchas collagen and basement membrane constituents, which contribute totissue damage.

There is increasing evidence that the bulk of tissue destruction inestablished dental lesions is a result of the mobilization of the hosttissues by an activation of monocytes, lymphocytes, and other hostcells. Engagement of these cellular elements by bacterial factors, inparticular bacterial lipopolysaccharide, is thought to stimulateproduction of both catabolic cytokines and inflammatory mediators suchas arachidonic acid and metabolites, such as prostaglandin E₂ (PGE₂).Such cytokines and inflammatory mediators, in turn, promote the releaseof tissue-derived enzymes. A summary of this reaction is described in anarticle, “The Pathogenesis of Periodontal Diseases”, Periodontal, April1999, Vol. 70, No. 4, pp. 457-470.

In some aspects, periodontal diseases are among the most unusualinfections of human beings. One reason for this uniqueness is theunusual anatomic feature wherein a mineralized structure, a tooth,passes through an integument so that a portion of the tooth is exposedto an external environment while a portion is within connected tissues.This unusual aspect of the infection is described in an article entitled“The Nature of Periodontal Diseases” by S. Socransky et al. in TheAnnals of Periodontology, vol.2, No. Mar. 1, 1997, pp. 4-10.

The tooth provides a surface for colonization by a diverse array ofbacterial species. Bacteria attach to the tooth itself as well as to theepithelial surface of the gingival or periodontal pockets, and tounderlying connective tissues. The outer layers of the tooth do notshed, and thus microbial colonization is facilitated. A situation isthen established wherein micro-organisms colonize a relatively stablesurface, which is the surface of the tooth, and are continually held inimmediate proximity to soft tissues of the periodontium.

The presence of the tooth increases the complexity of the host-parasiterelationship in a number of ways. The bacteria colonizing the tooth areby and large outside the body where they are less able to be controlledby mechanisms which operate within the tissues. The environment within aplaque is conducive to microbial survival, but it is unlikely to beparticularly an effective environment for a host to seek out and destroymicro-organisms.

Factors such as pH, eH and proteolytic enzymes affect performance ofhost defense mechanisms. In addition, the tooth provides sanctuary inwhich micro-organisms hide, persist at low levels during treatment, andthen re-emerge to cause further problems. Bacteria in dentin alluvials,which are flaws in the tooth, or areas which were demineralized bybacteria, are not easily approached by much larger host cells. In asimilar manner, non-cellular host factors face diffusion barriers.Mechanical debridement, other than vigorous removal of tooth material,cannot reach organisms in the tooth. Chemotherapeutic agents also havedifficulty in reaching the bacterial species. In particular,antimicrobial agents which require bacteria to multiply are adverselyaffected since the rate of growth is suspected to be very low.

One method for measuring the severity of periodontal disease is atechnique of periodontal probing depth (PD). Measuring periodontalprobing depth measures a loss of connective tissue attachments. A methodof periodontal probing has been described in an article entitled“Periodontal Probing: Probe-tip Diameter*”, published by the School ofDentistry, Medical College of Georgia, Augusta, Ga.

Periodontal probing is performed when a periodontist places a probe intothe sulcus or clinical pocket, and applies a force to move it apicallyinto tissue along a tooth surface. The clinician applies pressure on thetissue and when the tissue exerts an opposite, equal pressure to theprobe, displacement of the probe into the tissue will cease. Thepressure exerted by the probe is directly proportional to force on theprobe and inversely proportional to the area at the probe tip. With around probe, a change in the tip diameter has a greater effect onpressure than does a similar change in the force. An increase in theprobing force increases the pressure by a proportional amount. However,a relatively similar increase of the probe diameter reduces the pressureby a proportional amount which is squared. If the force is doubled (20to 40 gramforce), the pressure is increased by a factor of 2. If thediameter is doubled (0.4 to 0.8 millimeters), the pressure is reduced bya factor of 4. The pressure is equal to the force applied in theprobe/area at the tip-end=F/ur²=F/u(D/2)²: R=radius, D=diameter.

Positioning of the probe is shown in schematic cross-section in FIG. 1.The probe 10 is inserted in an area between connective tissue 12 anddentin 14, as is shown in FIG. 1. The depth 16 of the probe 10 into thatspace is a measure of the severity of periodontal disease.

In early periodontitis, gums appear similar to those in gingivitis.However, the seal around a tooth has been destroyed and the bone isstarting to eat itself away. This is an attempt by the body to escapeadvancing bacterial invasion. At this time, pockets are 4 to 5millimeters deep.

In moderate periodontitis, the infection has eaten away more bone. Gumsare receding, exposing root surfaces. Pus may be present. Pockets are upto about six millimeters deep. At this state of infection, the infectionmay still be treated non-surgically. However, once the bone is lost, itdoes not grow back. The teeth are weakened by partial loss of thesupporting bone. In advanced periodontitis, bone loss becomes moresevere. The gum tissue has now become more like scar tissue. The scartissue must be cut out surgically to get ride of the pockets. Advancedperiodontal pockets usually measure more than 6 millimeters.

Treatment regimens for periodontal disease typically involve removal ofmechanical irritants, such as plague and calculus, and removal of asmany bacteria as possible. The tissues are made as cleansable and ashealthy as possible. The patient is taught to keep teeth and gums clean.Non-surgical treatment includes scaling and root cleaning, which is deeproot cleaning of teeth to physically remove all tartar and plaque. Theteeth are polished to remove stains and to make the teeth harder for theplaque to adhere to. Prescription and non-prescription medications areapplied to the gums. Mouth rinses are used in conjunction with improvedhome care. Antibiotics are sometimes used.

Kakwarf et al., in an article entitled “Cytologic Evaluation of GingivalCurettage Facilitated by a Sodiumhypochloride Solution”, InternalPeriodontology, February 1992, pp. 63-69, describes a use of aninstrument against a gingival side of a pocket, in order to scrape anddebride soft tissue. The purpose of this scraping and debriding is toremove inflamed tissue and to maintain teeth and gums in a state ofperiodontal health. In some treatments, sodium hypochlorite solution wasintroduced along with the curettage in order to remove all theepithelium from a pocket. Citric acid treatment has also been used toaugment epithelial treatment.

Local controlled delivery of antibiotics has also been performed inconjunction with scaling and root cleaning. One antibiotic deliveredthrough a controlled release mechanism is doxycycline hyclate. This typeof treatment was described in an article written by Garret et al.,entitled “The Effect of Locally-delivered Controlled ReleaseDioxycycline on Scaling and Root Cleaning on Periodontal MaintenancePatients over Nine Months”, Periodontal Period, Vol. 71, No. 1 January1, 2000, pp. 2-9. Other antibiotics delivered through this type offormat include the tetracycline.

In cases of advanced periodontal disease, the gum adjacent to thediseased tooth is lifted from the tooth and bone, and diseased tissue isremoved. The infected bone may also be reshaped. After surgery, the gumis repositioned and sutured into place.

In some cases, destroyed tissue between teeth or roots is partiallyregenerated. Once damaged area of tissue is removed and specialmembranes are inserted, new tissue grows over a period of weeks tomonths. This type of regeneration, as measured by a probe test,typically results in a decrease in probe depth of only about 1millimeter.

DESCRIPTION OF THE DRAWINGS

FIG. 1 illustrates a cross-sectional view of one embodiment of a probedtooth with periodontal disease.

FIG. 2 is a view of the components of the treatment solution of thepresent invention.

FIG. 3 is a top plan view of the needle of the present invention.

FIG. 4 is a side view of the diseased tooth, tooth pocket and positionof the needle of the present invention.

FIG. 4A is a side view of the needle in a periodontal pocket.

FIG. 4B is a side view of the needle with dual ports within theperiodontal pocket.

FIG. 5 is a perspective view of one kit embodiment.

SUMMARY OF THE INVENTION

One embodiment of the present invention includes a method for treatingperiodontal disease. The method comprises delivering to a pocket of atooth with periodontal disease, a viscous, reddish-brown solutioncomprising sulfuric acid and sulphonated phenolic compounds. The methodalso includes retaining the reddish-brown solution in the pocket for atime ranging from about 5 seconds to about 60 seconds.

Another embodiment of the present invention includes a method for savingcondemned teeth. The method comprises delivering to a pocket of a toothwith periodontal disease, a viscous, reddish-brown solution comprisingsulfuric acid and sulphonated phenolic compounds. The method alsoincludes retaining the reddish-brown solution in the pocket for a timeranging from about 5 seconds to about 60 seconds.

One other embodiment of the present invention includes a needle fordelivering a treatment solution for periodontal disease. The needlecomprises a deformable main body that defines a side hole for deliveryof the treatment solution.

Another embodiment of the present invention includes a kit for treatingperiodontal disease. The kit comprises a container with a treatmentsolution comprising a viscous, reddish-brown solution comprisingsulfuric acid and sulphonated phenolic compounds. The kit also comprisesa needle for delivering the treatment solution to a pocket of a diseasedtooth.

DETAILED DESCRIPTION

One method aspect of the present invention includes a method fortreating periodontal disease. The method comprises providing a syringe,with a needle, such as is shown at 30 in FIG. 3 and providing areddish-brown, sulphonated phenolic solution, ingredients of which areshown in FIG. 2. The method includes performing a conventional scale andplaning treatment. Scaling removes calculus and plaque on a tooth.Planing is a rubbing against the root of the tooth, such as is shown at40 in FIG. 4. Next, using a syringe and syringe needle of the presentinvention 30, water is delivered to a pocket 42 of the scaled and planedtooth. Water is added until the water is expressed at least one portionof a circumferential interface 44 where the gum meets the tooth 40.Expressed water is removed from the patient's mouth by suction.

A second syringe is loaded with the reddish-brown, sulphonated phenolicsolution. The needle of the present invention 30 is installed on thesyringe. The needle is inserted into the pocket of the tooth and thereddish-brown, sulphonated phenolic solution is delivered to the pocket.

The sulphonated phenolic solution is added until the solution isexpressed in about the same location as the water had been expressed.The sulphonated phenolic solution is retained in the pocket 42 for aperiod of time ranging from about 10 seconds to about 60 seconds.Suction is then applied at the point of expression in order to removethe sulphonated phenolic solution. Water is then added to the pocket inorder to rinse any remaining sulphonated phenolic solution from thepocket. The water is added until liquid expressed is clear. Expressedliquid is removed by suction.

For some method embodiments, high pressure water is then added to thepocket 42. The high pressure water irrigates the pocket 42 and removesall necrotic debris from within the infected area. Antibiotic treatment,typically employed in treatment of periodontal disease, is not necessarywith the method of the present invention.

It has surprisingly been found that the method of the present inventionnot only substantially eliminates pain associated with periodontaldisease, but appears to reverse tissue damage and destruction caused byetiological agents of periodontal disease. In particular, it has beenobserved that following treatment with the method of the presentinvention, even teeth such as condemned teeth, are salvageable. This isa heretofore unobserved phenomenon. It is even more surprising thatthese remarkable results are achievable without a use of antibiotics.

It is not understood exactly how the method of the present invention isable to initiate tissue regeneration. It is believed that the ability ofthe sulphonated phenolic compound to remove necrotic and other diseasedtissue while preserving healthy tissue at the interface is responsiblefor rapid tissue regeneration. It is not known whether tissueregeneration includes regeneration of the ligament or surroundingmucosal tissue or both. It has been observed, however, that probe depthis decreased by a length of up to about 5 millimeters followingtreatment! Successful treatments using regimens described herein, suchas time release of antibiotics, have been regarded as successful ifprobe depth reduction was about 1 millimeter. No method of periodontaltreatment heretofore known has been able to salvage condemned teeth, asis the case with the method of the present invention.

One other benefit of the method of the present invention is that it is asingle treatment-based method. It is not necessary to install anappliance which engages in continuous release of drugs. After the singletreatment, remaining tissue is in a condition wherein it is able toregenerate on its own. Because of the rapidity of regeneration and thehealth of the surrounding and remaining tissue, bacterial reinfectiondoes not occur, provided the patient engages in good oral hygiene.Consequently, follow up antibiotic treatment is not necessary.

As used herein, the viscous, sulphonated phenolic compound refers toDebacterol, a mixture of 50% sulfuric acid, 4% sulfonated phenol and 24%sulfonated phenolics, including guaiacol, resol, creosol and xylenol inan aqueous solution, which is manufactured by Northern ResearchLaboratories, Inc., of 8400 Normandale Lake Blvd., Suite 920, ofMinneapolis Minn. 55437-1085. The viscous, sulphonated phenolic compoundcomprises the following ingredients in the following concentrations:

Sulphonated Compound Group Weight % Phenol 2.5 to 7.5 Cresols   5 to 7.5Creosols  5 to 15 Xylenol   5 to 7.5 Guaiacol  5 to 15

One specific embodiment had the following concentration ranges:

Sulphonated Compound Group Weight % Phenol 3.10 to 4.94 Guaiacol  9.14to 14.56 Cresol 3.49 to 5.56 Creosol 3.81 to 6.07 Xylenol 4.52 to 7.21Total 24.06 to 38.34

A breakdown of phenolic compounds in this aqueous solution is shown inFIG. 1. The source of the Debacterol phenolic components is beechwoodcreosote. The Debacterol solution has a dark reddish-brown color thatrenders the material visible when applied to the lesion and surroundinghealthy tissue. Specific phenolic components include sulfonated phenol,4-methoxyphenol (Gualacol), 3,4-xylenol, and o-cresol.

The Debacterol density is 1.08 gms per ml at 20 degrees Centigrade. Thedistillation range is 200 to 230. The flash point is about 99 degreesCentigrade. Debacterol has a percent moisture of about 10 to 19%, anacidity as (mg/kg)calcium carbonate of 480,000 to 487,000 and a percent4-OH benzene sulfonic acid, wt./wt. of 3.2 to 4.5.

As used herein, “condemned teeth” refers to teeth associated with suchsevere periodontal disease that the teeth are regarded as not capable ofbeing saved. Condemned teeth are typically extracted.

As used herein “probe depth” refers to a measurement of a loss ofconnective tissue attachments. In early gingivitis, probe depth is about4 to 5 millimeters. With moderate periodontitis, probe depth is about 6millimeters. For advanced periodontal disease, probe depth is greaterthan 6 millimeters.

As used herein, “periodontal disease” refers to a loss of supportingtissues of the teeth.

One embodiment of the syringe needle of the present invention isillustrated at 30 in FIG. 3. The syringe needle 30 has a first port 32and a second port 34 staggered with respect to the first port. Theneedle is made of a deformable material that permits the syringe needleto be positioned within the diseased pocket of a tooth. The syringeneedle terminates in a tip 36. The sideholes 32 and 34 permit a moredesirable flushing and introduction of fluids into the pocket. While aneedle with two staggered ports is described herein, it is understoodthat a needle with a single port in usable in the method of the presentinvention. A needle with more than two ports is also usable for somemethod embodiments of the present invention.

The needle 30 is made from a material that permits reuse of the needle30 and that is somewhat deformable. To be reused, the needle materialmust be autoclavable. Suitable needle materials include nitinol,stainless steel, and polymeric materials.

One other embodiment of the present invention includes a kit fortreating periodontal disease. The kit comprises a container, thecontainer 50 containing the viscous, reddish-brown sulfonated phenolicsolution and a needle 30 for delivering the solution to a diseasedpocket of a tooth. The kit also comprises, for some embodiments, asyringe and a container that contains sterile water. Each of thecontainers and the needle and the syringe, if present, is packaged in alarger container that encloses all of these items.

Although water is described herein as a rinse agent used in the methodof the present invention, it is understood that aqueous solutionscomprising additional components such as sodium carbonate, sodiumcitrate, sodium chloride and antibiotic components are also usable.

Since the invention disclosed herein may be embodied in other specificforms without departing from the spirit or general characteristicsthereof, some of which forms have been indicated, the embodimentsdescribed herein are to be considered in all respects illustrative andnot restrictive. The scope of the invention is to be indicated by theappended claims, rather than by the foregoing description, and allchanges, which come within the meaning and range of equivalency of theclaims, are intended to be embraced therein.

What is claimed is:
 1. A method for treating periodontal disease,comprising: providing a device for delivering a reddish-brown solutioncomprising sulfuric acid and sulphonated phenolic compounds; deliveringto a pocket of a tooth with periodontal disease, a viscous,reddish-brown solution comprising sulfuric acid and sulphonated phenoliccompounds using the device; and retaining the reddish-brown solution inthe pocket for a time ranging from about 5 seconds to about 60 seconds.2. The method of claim 1 and further comprising pretreating the tooth byscraping and planing the tooth prior to delivering the reddish-brownsolution.
 3. The method of claim 1 and further comprising rinsing thepocket of the tooth with water or other aqueous solution prior to addingthe reddish-brown solution.
 4. The method of claim 1 and furthercomprising rinsing the pocket of the tooth with water or other aqueoussolution after adding the reddish-brown solution.
 5. The method of claim1 and further comprising removing the reddish-brown solution byapplication of suction.
 6. The method of claim 1 and further comprisingproviding a syringe needle for delivering the reddish-brown solution. 7.A method for saving condemned teeth, comprising: delivering to a pocketof condemned tooth, a viscous, reddish-brown solution comprisingsulfuric acid and sulphonated phenolic compounds; and retaining thereddish-brown solution in the pocket for a time ranging from about 5seconds to about 60 seconds.
 8. The method of claim 7 further comprisingrinsing the pocket of the condemned tooth with water or other aqueoussolution prior to adding the reddish-brown solution.
 9. The method ofclaim 7 and further comprising rinsing the pocket of the condemned toothwith water or other aqueous solution after adding the reddish-brownsolution.
 10. A kit comprising: a first container containing a viscous,reddish-brown sulfonated phenolic solution; and a syringe needle; acontainer for enclosing the first container and the syringe needle; anda second container for containing an aqueous rinse solution.